Balaji C, Muthukumaran J, Nalini N
Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, Tamil Nadu, India.
Department of Biochemistry and Biotechnology, Faculty of Science, Annamalai University, Annamalainagar, Tamil Nadu, India
Hum Exp Toxicol. 2014 Dec;33(12):1253-68. doi: 10.1177/0960327114522501. Epub 2014 Feb 14.
Sinapic acid (SA) is a naturally occurring phenolic acid found in various herbal plants which is attributed with numerous pharmacological properties. This study was aimed to investigate the chemopreventive effect of SA on 1,2-dimethylhydrazine (DMH)-induced rat colon carcinogenesis. Rats were treated with DMH injections (20 mg kg(-1) bodyweight (b.w.) subcutaneously once a week for the first 4 consecutive weeks and SA (20, 40 and 80 mg kg(-1) b.w.) post orally for 16 weeks. At the end of the 16-week experimental period, all the rats were killed, and the tissues were evaluated biochemically. Our results reveal that DMH alone treatment decreased the levels/activities of lipid peroxidation by-products such as thiobarbituric acid reactive substances, conjugated dienes and antioxidants such as superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase and reduced glutathione in the intestine and colonic tissues which were reversed on supplementation with SA. Moreover, the activities of drug-metabolizing enzymes of phase I (cytochrome P450 and P4502E1) were enhanced and those of phase II (glutathione-S-transferase, DT-diaphorase and uridine diphosphate glucuronosyl transferase) were diminished in the liver and colonic mucosa of DMH alone-treated rats and were reversed on supplementation with SA. All the above changes were supported by the histopathological observations of the rat liver and colon. These findings suggest that SA at the dose of 40 mg kg(-1) b.w. was the most effective dose against DMH-induced colon carcinogenesis, and thus, SA could be used as a potential chemopreventive agent.
芥子酸（SA）是一种天然存在的酚酸，存在于多种草药植物中，具有多种药理特性。本研究旨在探讨SA对1,2-二甲基肼（DMH）诱导的大鼠结肠癌发生的化学预防作用。大鼠连续4周每周皮下注射一次DMH（20 mg kg⁻¹体重（b.w.）），并口服SA（20、40和80 mg kg⁻¹ b.w.）16周。在16周实验期结束时，处死所有大鼠，并对组织进行生化评估。我们的结果显示，单独使用DMH治疗会降低肠道和结肠组织中脂质过氧化副产物如硫代巴比妥酸反应性物质、共轭二烯的水平/活性以及超氧化物歧化酶、过氧化氢酶、谷胱甘肽还原酶、谷胱甘肽过氧化物酶和还原型谷胱甘肽等抗氧化剂的水平/活性，而补充SA后这些指标会逆转。此外，单独接受DMH治疗的大鼠肝脏和结肠黏膜中I相药物代谢酶（细胞色素P450和P4502E1）的活性增强，II相药物代谢酶（谷胱甘肽-S-转移酶、DT-黄递酶和尿苷二磷酸葡萄糖醛酸转移酶）的活性降低，补充SA后这些变化会逆转。大鼠肝脏和结肠的组织病理学观察结果支持了上述所有变化。这些发现表明，40 mg kg⁻¹ b.w剂量的SA是对抗DMH诱导的结肠癌发生最有效的剂量，因此，SA可作为一种潜在的化学预防剂。
